COPD

Scientists have long suspected that respiratory viruses play a critical role in the development of chronic lung diseases such as asthma and chronic obstructive pulmonary disease (COPD). Studying mouse and cell models of this process, researchers now have shown how immune cells dispatched to the lung to destroy a respiratory virus can fail to disperse after their job is done, setting off a chain of inflammatory events that leads to long-term lung problems.

In cells lining the airway, high levels of certain proteins have long been linked with the overproduction of mucus characteristic of diseases like asthma and COPD. New research from the School of Medicine provides clues to potentially counteract inappropriate mucus production.

Your nose is not the only organ in your body that can sense cigarette smoke wafting through the air. Scientists at Washington University in St. Louis have shown that your lungs have odor receptors as well. The odor receptors in your lungs are in the membranes of flask-shaped neuroendocrine cells that dump neurotransmitters and neuropeptides when the receptors are stimulated, perhaps triggering you to cough to rid your body of the offending substance.

School of Medicine researchers have described another link in the chain of events that connects acute viral infections to the development of chronic obstructive pulmonary disease (COPD). Their discovery points to a new therapeutic target for COPD, an extremely common disease of the lower airways. The image depicts airway epithelial cells from lung tissue of a COPD patient.

Respiratory conditions that restrict breathing such as asthma and chronic obstructive pulmonary disease (COPD) are common killers worldwide. But no effective treatments exist to address the major cause of death in these conditions — excess mucus production. Now, Washington University researchers have described the molecular pathway responsible for excess mucus in airway cells and have used that information to design a series of new drugs that inhibit that pathway.

Your DNA influences how much you smoke and whether you will develop lung cancer or chronic obstructive pulmonary disease. A study, led by researchers at Washington University School of Medicine, is the first large-scale effort to match genetics with smoking, lung cancer and COPD combined. The investigators studied 38,000 smokers and found that two groups of gene variants on chromosome 15 influence the risk for all three problems.

A drug commonly used for the treatment of chronic obstructive pulmonary disease (COPD) successfully treats adults whose asthma is not well controlled on low doses of inhaled corticosteroids, says a new study.